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Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What stimulates the pituitary gland to release hormones?

A

Hormones released from the hypothalamus

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2
Q

What hormones are released from the anterior pituitary?

A
  • Thyroid stimulating hormone (TSH)
  • Adenocorticotropic hormone (ACTH)
  • Follicle-stimulating hormone (FSH)
  • Lutienizing hormone (LH)
  • Growth hormone (GH)
  • Prolactin
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3
Q

What hormones are released from the posterior pituitary?

A
  • Oxytocin

- Anti-diuretic hormone (ADH)

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4
Q

What hormones are released from the hypothalamus?

A
  • Thyrotropin-releasing hormone (TRH)
  • Corticotrophin-releasing hormone (CRH)
  • Growth hormone releasing hormone (GHRH)
  • Gonadotropin-releasing hormone (GRH)
  • Dopamine
  • Somatostatin
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5
Q

How does the thyroid hormone axis work?

A
  • TRH released from hypothalamus in response to low T3 + T4
  • Anterior pituitary release TSH
  • TSH works on thyroid to stimulate T3 + T4 (triiodothyronine + thyroxine) release
  • Negative feedback-> T3 + T4 suppress TRH + TSH release
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6
Q

How does the adrenal hormone axis work?

A
  • Hypothalamus released CRH in response to low cortisol
  • Anterior pituitary released ACTH
  • Adrenal glands stimulated to release cortisol
  • Negative feedback-> high cortisol suppressed CRH release
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7
Q

What are the functions of cortisol?

A
  • Stress hormone-> released in pulses in response to stimulus
  • Inhibit immune system + bone formation
  • Increase metabolism + alertness
  • Raises blood glucose levels
  • Diurnal variation-> peak in morning + lowest in evening
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8
Q

When are cortisol levels highest in the body?

A

In the morning

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9
Q

When are cortisol levels lowest in the body?

A

In the evening

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10
Q

How does the growth hormone axis work?

A
  • GHRH released from hypothalamus
  • GH released from anterior pituitary and acts on cells
  • Stimulates insulin-like growth factor (IGF-1) from liver
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11
Q

What are the functions of growth hormone?

A
  • Acts on all cells
  • Stimulate muscle growth
  • Increases bone density and strength
  • Stimulates cell regeneration + reproduction
  • Stimulates internal organ growth
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12
Q

How does the parathyroid hormone axis work?

A
  • Low serum calcium, low magnesium + high serum phosphate
  • Stimulates PTH release from the 4 parathyroid glands
  • Increases serum calcium
  • Negative feedback loop
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13
Q

What are the functions of parathyroid hormone (PTH)?

A
  • Increase activity and number of osteoclasts-> reabsorption of calcium from bone to blood
  • Increased calcium reabsorption in the kidney-> less excreted
  • Stimulates conversion of vitamin D3 to calcitriol in kidneys-> to promote calcium absorption in the small intestine
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14
Q

How does the renin-angiotensin aldosterone (RAAS) system work?

A
  • Low blood pressure
  • Detected by juxtaglomerular cells in afferent (+ some efferent) arterioles in the kidney-> release renin
  • Renin converts antigiotensinogen (from liver) to angiotensin I
  • Angiotensin I converted to angiotensin II (in lungs) by angiotensin converting enzyme (ACE
  • Angiotensin II acts on vessels to vasoconstrict-> increase BP
  • Angiotensin II also stimulates release of aldosterone
  • Aldosterone-> increase sodium reabsorption from distal tubule-> increases BP
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15
Q

How does angiotensin II increase blood pressure?

A
  • Acts on blood vessels to vasoconstrict

- Stimulates release of aldosterone

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16
Q

What is the function of aldosterone?

A
  • Mineralocorticoid steroid released from adrenal glands-> increases BP
  • Acts on distal tubule-> increase sodium reabsorption + potassium secretion
  • Acts on collecting ducts-> increase hydrogen secretion
  • As sodium is reabsorbed-> increases intravascular volume + increases BP
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17
Q

What is Cushing’s syndrome?

A

Signs and symptoms due to prolonged abnormal cortisol elevation

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18
Q

What is Cushing’s disease?

A

Pituitary adenoma secretes excess ACTH and causes Cushing’s syndrome

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19
Q

What is the difference between Cushing’s syndrome and Cushing’s disease?

A
  • Syndrome-> signs and symptoms due to prolonged abnormal cortisol elevation
  • Disease-> pituitary adenoma secretes excess ACTH and causes Cushing’s syndrome
  • So disease causes syndrome, but syndrome not necessarily due to disease
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20
Q

What are the features of Cushing’s syndrome?

A

Central obesity, moon face, abdominal striae, buffalo hump, proximal limb muscle wasting, hypertension, easy bruising, poor skin healing, insomnia, depression, T2DM, cardiac hypertrophy

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21
Q

What are the causes of Cushing’s syndrome?

A
  • Exogenous steroids
  • Cushing’s disease
  • Adrenal adenoma
  • Paraneoplastic-> excess ACTH from cancer eg small cell lung cancer
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22
Q

What is the investigation of choice for Cushing’s syndrome?

A

Dexamethasone suppression test

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23
Q

How does the dexamethasone suppression test work?

A
  • Give low dose dexamethasone (1mg) dose at night + measure cortisol and ACTH in the morning
  • Normal result-> morning spike should be suppressed by dexamethasone (as lower CRH + ACTH output so lower cortisol)
  • Abnormal result-> not suppressed + indicated Cushing’s
  • Give high dose dexa (8mg) to find out cause
  • If cortisol suppressed + ACTH suppressed (ie some response to negative feedback)-> pituitary adenoma
  • If cortisol not suppressed + ACTH suppressed-> adrenal adenoma
  • If cortisol + ACTH not suppressed-> ectopic ACTH
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24
Q

What result of a dexamethasone suppression test would indicate Cushing’s syndrome?

A

Normal morning spike of cortisol not suppressed after giving low dose dexa the night before

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25
Q

What result of a dexamethasone suppression test would indicate pituitary adenoma?

A
  • Normal morning spike of cortisol not suppressed after giving low dose dexa the night before
  • Cortisol and ACTH suppressed after high dose dexa-> some response to negative feedback
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26
Q

What result of a dexamethasone suppression test would indicate adrenal adenoma?

A
  • Normal morning spike of cortisol not suppressed after giving low dose dexa the night before
  • Cortisol not suppressed + ACTH suppressed after high dose dexa given
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27
Q

What result of a dexamethasone suppression test would indicate ectopic ACTH release?

A
  • Normal morning spike of cortisol not suppressed after giving low dose dexa the night before
  • Cortisol + ACTH not suppressed
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28
Q

What investigations are done in Cushing’s syndrome?

A
  • Dexamethasone suppression test
  • Bloods-> FBCs, U+Es (hypokalaemia when aldosterone released by adenomas)
  • 24 hour urinary free cortisol
  • MRI brain-> pituitary adenoma
  • Chest CT-> small cell lung cancers
  • Abdominal CT-> adrenal tumours
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29
Q

How is Cushing’s syndrome treated?

A
  • Treat the underlying cause-> remove pituitary/adrenal adenomas etc
  • Can remove adrenals + give replacement steroids
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30
Q

What happens in adrenal insufficiency?

A

Adrenals don’t produce enough cortisol + aldosterone-> life threatening

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31
Q

What are the broad causes of adrenal insufficiency?

A
  • Addison’s disease-> primary adrenal insufficiency (usually AI)
  • Secondary-> loss/damage to pituitary causes inadequate ACTH release
  • Tertiary-> usually steroids causing inadequate CRH release from hypothalamus
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32
Q

What are the causes of primary adrenal insufficiency?

A

Addision’s disease-> autoimmune usually

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33
Q

What are the causes of secondary adrenal insufficiency?

A

Loss or damage to pituitary-> surgery, infection, hypoperfusion, radiotherapy, Sheehan’s (blood loss in childbirth causing pituitary glad necrosis)

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34
Q

What are the causes of tertiary adrenal insufficiency?

A

Long term steroids (3+ weeks)-> sudden withdrawal can lead to inadequate endogenous steroid production

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35
Q

What are the symptoms and signs of adrenal insufficiency?

A
  • Fatigue, nausea, cramps, abdominal pain, reduced libido
  • Hypotension
  • Bronze hyperpigmentation of creases-> ACTH stimulates melanin production from melanocytes
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36
Q

What is the investigation of choice for adrenal insufficiency?

A

Short synacthen test (ACTH stimulation test)

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37
Q

How does the short synacthen (ACTH stimulation) test work?

A
  • Give synacthen (synthetic ACTH)
  • Measure cortisol at baseline, 30 and 60 minutes after
  • Normal-> level doubles or more
  • Addison’s (primary)-> failure to double
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38
Q

How does the long synacthen test work and when is it used?

A
  • To distinguish between primary and secondary adrenal insufficiency
  • Give ACTH infusion
  • Primary-> no response
  • Secondary-> eventually rises (adrenal atrophy)
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39
Q

How is adrenal insufficiency investigated?

A
  • Short synacthen test
  • Long synacthen test-> distinguish types
  • ACTH level measured
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40
Q

How is adrenal insufficiency treated?

A
  • Hydrocortisone-> cortisol replacement
  • Fludrocortisone-> aldosterone replacement
  • Steroid card + emergency ID tag-> indicate lifelong steroids
  • Steroid doses doubled in acute illness
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41
Q

What is Addisonian/adrenal crisis?

A

Acute presentation of severe Addison’s?

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42
Q

What are the symptoms and signs of Addisonian/adrenal crisis?

A

LOC, hypotension, hypoglycaemia, hyponatraemia, hyperkalaemia

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43
Q

What can trigger Addisonian/adrenal crisis?

A
  • Can be first presentation of Addison’s

- Infection, trauma, acute illness, withdrawal of steroids

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44
Q

How is Addisonian/adrenal crisis managed?

A
  • IV hydrocortisone 100mg stat then 100mg every 6 hours
  • IV fluids
  • Hypoglycaemia correction
  • Monitoring of electrolytes and fluids
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45
Q

What antibodies can be raised in thyroid disease?

A
  • Anti-TPO-> Grave’s and Hashimoto’s thyroiditis
  • Antithyroglobulin-> normal, Grave’s, Hashimotos, thyroid cancer
  • TSH receptor antibodies-> Grave’s
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46
Q

What are anti-TPO antibodies and when can they be raised?

A
  • Antithyroid peroxidase antibodies

- Grave’s and Hashimoto’s thyroiditis

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47
Q

What are antithyroglobulin antibodies and when can they be raised?

A
  • Against thyroglobulin-> protein produced by the thyroid

- In normal, Grave’s, Hashimotos, thyroid cancer

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48
Q

What are TSH receptor antibodies and when are they raised?

A
  • Cause of Grave’s disease

- Mimic TSH and bind to receptors-> stimulate thyroid hormone release

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49
Q

What imaging can be used to investigate thyroid pathology?

A
  • US + guided biopsy-> between cystic and solid nodules

- Radioisotope scans-> iodine given oral/IV + taken up by thyroid cells, more function when hyperthyroid or cancers

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50
Q

What might a radioisotope scan show in thyroid disease?

A
  • Grave’s-> diffuse high uptake
  • Toxic multinodular goitre-> focal high uptake
  • Cancer-> might be ‘cold’ ie low
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51
Q

What is primary hyperthyroidism?

A

Overproduction of thyroid hormones due to pathology in the thyroid itself

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52
Q

What is secondary hyperthyroidism?

A

Overproduction of thyroid hormones due to overstimulation/overproduction of TSH-> hypothalamus or pituitary pathology

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53
Q

What are the features of hyperthyroidism (in general)?

A

Anxiety, sweating, heat intolerance, tachycardia, weight loss, fatigue, loose stools, sexual dysfunction

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54
Q

What is Grave’s disease?

A

Autoimmune disease-> TSH receptor antibodies produced which mimics TSH and causes T3/T4 overproduction

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55
Q

What are some of the symptoms and signs of Grave’s disease?

A
  • Anxiety, sweating, heat intolerance, tachycardia, weight loss, fatigue, loose stools, sexual dysfunction
  • Diffuse goitre without nodules
  • Exophthalmos-> bulging eyeballs due to inflammation + hypertrophy of tissue behind the eyeballs
  • Pretibial myxoedema-> waxy + discoloured + oedematous, due to TSH-receptor antibodies causing mucin deposits under skin
  • Diffuse goitre without nodules
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56
Q

What is toxic multinodular goitre?

A

Nodules in the thyroid act independently from normal negative feedback-> produce excess hormones

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57
Q

What are the features of toxic multinodular goitre?

A
  • Anxiety, sweating, heat intolerance, tachycardia, weight loss, fatigue, loose stools, sexual dysfunction
  • Goitre with firm nodules
  • Often 50+
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58
Q

What are solitary toxic thyroid nodules?

A

Benign adenomas producing thyroid hormones

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59
Q

How are solitary toxic thyroid nodules treated?

A

Surgical removal

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60
Q

What is De Quervain’s thyroiditis?

A

A viral infection causing hyperthyroidism then hypothyroidism as TSH levels fall (due to negative feedback)

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61
Q

What are the symptoms and signs of De Quervain’s thyroiditis?

A

Fever, neck pain, tenderness, dysphagia, hyperthyroidism

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62
Q

How is De Quervain’s thyroiditis managed?

A
  • Usually self limiting

- Supportive-> NSAIDs for pain, beta blockers for hyperthyroid

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63
Q

What is a thyroid storm and what are its features?

A

Rare presentation of thyrotoxic crisis-> pyrexia, tachycardia, delirium

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64
Q

How is thyroid storm managed?

A
  • Admission and monitoring
  • Anti-arrhythmias
  • Beta-blockers
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65
Q

How is hyperthyroidism managed?

A
  • Carbimazole-> may lead to complete remission in 18 months
  • Propylthiouracil-> 2nd line anti-thyroid
  • Radioactive iodine-> destroy cells and can cause remission in 6 months
  • Beta-blockers eg propranolol-> reduce adrenergic symptoms
  • Surgery-> thyroid or nodules, will need levothyroxine for life
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66
Q

What two methods of carbimazole therapy are used in hyperthyroidism?

A
  • Titration-block-> dose altered till normal TFTs

- Block + replace with levothyroxine

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67
Q

What should patients be told when given radioactive iodine therapy in hyperthyroidism?

A
  • Avoid when pregnant/trying

- Limit contact with anyone for a few days after therapy

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68
Q

What is Hashimoto’s thyroiditis?

A
  • Autoimmune inflammation for thyroid-> associated with anti-TPO and antithyroglubulin antibodies
  • Goitre then atrophy of gland
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69
Q

What are the causes of hypothyroidism?

A
  • Hashimoto’s thyroiditis
  • Iodine deficiency
  • Secondary to hyperthyroid treatments
  • Medications-> lithium, amiodarone
  • Hypopituitarism-> tumour, infection, vascular (eg Sheehan’s), radiation
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70
Q

How does hypothyroidism present?

A

Weight gain, fatigue, dry skin, coarse hair, hair loss, fluid retention, heavy/irregular periods, constipation

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71
Q

What are the investigations for hyperthyroidism?

A

TFTs

  • Primary-> low TSH and high T3/T4
  • Secondary-> high TSH and high T3/T4
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72
Q

What are the investigations for hypothyroidism?

A

TFTs

  • Primary-> high TSH + low T3/T4
  • Secondary-> low TSH + low T3/T4
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73
Q

How is hypothyroidism managed?

A

Levothyroxine-> synthetic T3 that metabolises to T3 in body

  • Dose titrated till TSH levels normal
  • Measured monthly till stable then less often
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74
Q

What is the ideal blood glucose concentration in a healthy patient?

A

4.4-6.1mmol/L

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75
Q

Where is insulin produced?

A

Beta cells in the islets of Langerhans-> in the pancreas

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76
Q

How does insulin work?

A
  • Anabolic ie building hormone
  • Cause cells in body to absorb glucose + use as fuel
  • Cause muscle and liver cells to absorb glucose and store as glycogen
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77
Q

Where is glucagon produced?

A

Alpha-cells in islets of Langerhans-> in pancreas

78
Q

How does glucagon work?

A
  • Catabolic ie breakdown hormone
  • Released in response to low blood sugars and stress
  • Tells liver to break glycogen into glucose (glucogenolysis) and convert proteins and fats to glucose (gluconeogenesis)
79
Q

What is ketogenesis?

A
  • When insufficient glucose supply and glycogen stores are exhausted due to prolonged fasting
  • Liver takes fatty acids + converts to ketones-> can use as fuel in the brain
  • Ketones normal when fasting or low carb/high fat diet-> buffered
  • Can be abnormal-> DKA etc
80
Q

What are ketones?

A

Water soluble fatty acids-> converted in the liver and can cross BBB to fuel brain

81
Q

What is the pathophysiology of type 1 diabetes?

A
  • Pancreas stops producing insulin
  • Cells can’t take glucose from blood + use as fuel-> body thinks being fasted + causes hyperglycaemia
  • Can be genetic or due to viruses (Coxsackie B, enterovirus)
82
Q

What is the management of type 1 diabetes (in general)?

A
  • Lifelong subcubtaneous insulin-> usually long and short acting
  • Monitoring of dietary carbs + blood glucose
83
Q

What advice should be given to patients taking SC insulin?

A

Cycle the site you use-> lipodystrophy will mean not absorb insulin properly

84
Q

When should blood glucose levels be measured in type 1 diabetes?

A

Waking, before meals and before bed

85
Q

When is short-acting insulin usually administered?

A

30 minutes before meals

86
Q

What does the HbA1c blood test show?

A
  • Glycated haemoglobin ie how much glucose attached
  • Over last 3 months (RBC lifespan)
  • Track progression + inverventions
87
Q

How can patients measure their own blood glucose?

A
  • Capillary BM monitoring

- Flash glucose monitoring eg Freestyle Libre

88
Q

How does flash glucose monitoring (eg Freestyle Libre) work?

A
  • Sensor on skin measures interstitial fluid glucose at short intervals
  • Lag of 5 minutes behind blood
  • Replace sensor every 2 weeks
  • Need additional BM monitoring if suspect hypo
89
Q

What are the symptoms of hypoglycaemia?

A

Tremor, sweating, irritable, dizziness, pallor, LOC, coma, death

90
Q

How is hypoglycaemia managed?

A
  • If conscious-> fruit juice or glucose gel + slow acting carbs
  • Drowsy-> IV glucose 10% or 20%
  • Can also use IM glucagon
91
Q

What is the pathophysiology of the complications of hyperglycaemia?

A

Long term exposure-> endothelial damage, leaky vessels + unable to regenerate, immune system suppression + increased infection risk-> micro and macrovascular complications

92
Q

What are the complications of prolonged hyperglycaemia in diabetes?

A
  • Macrovascular-> CAD, peripheral ischaemia (diabetic foot), stroke, HTN
  • Microvascular-> peripheral neuropathy, retinopathy, kidney disease (glomerulosclerosis)
  • Infections-> UTI, pneumonia, skin + soft tissue, fungal (candidiasis)
93
Q

What causes diabetic ketoacidosis?

A

In diabetics when not enough endogenous or exogenous insulin-> body unable to process glucose

94
Q

What is the pathophysiology behind diabetic ketoacidosis?

A
  • In diabetics when not enough endogenous or exogenous insulin-> body unable to process glucose
  • Cells think no fuel-> ketogenesis
  • Higher glucose + ketones-> bicarb produced in kidneys to counteract + balance pH
  • Over time-> ketones use up bicarb-> acidic blood (ketoacidosis)
  • Kidneys overwhelmed + glucose comes out in urine-> draws water out (osmotic diuresis)-> polyuria + dehydration
  • Polydipsia-> due to dehydration
  • Serum K+ can be high or normal-> total body K+ low as none stored in cells
95
Q

How does diabetic ketoacidosis present?

A
  • Polyuria, polydipsia, N+V, acetone smell on breath, dehydration, hypotension, altered consciousness, sepsis
  • Hyperglycaemia, dehydration, ketosis, metabolic acidosis, K+ imbalance
96
Q

What is the diagnostic criteria for diabetic ketoacidosis?

A
  • Hyperglycaemia-> >11mmol/L
  • Ketosis-> >3mmol/L
  • Acidosis-> pH <7.3
97
Q

What is the management for diabetic ketoacidosis?

A

FIG-PICK

  • Fluids-> 1L IV saline stat then 4L over next 12 hours
  • Insulin-> eg actarapid 0.1unit/kg/hour then start normal insulin regime before stopping IV
  • Glucose-> close monitoring + add dextrose infusion when below 14mmol/L
  • Potassium-> monitor + correct by <10mmol/hour
  • Infection-> treat if underlying
  • Chart-> fluid balance
  • Ketones-> monitor (or bicarb)
98
Q

What is the pathophysiology of type 2 diabetes?

A
  • Repeated exposure to glucose + insulin-> cells become resistant + takes more insulin to produce response
  • Beta-cells fatigued + damaged by producing insulin-> produce less
  • Chronic hyperglycaemia-> complications
99
Q

What are the risk factors for type 2 diabetes?

A

Older age, BAME, family history, obesity, sedentary, high carbs

100
Q

How does type 2 diabetes typically present?

A

Fatigue, polyuria, polydipsia, weight loss, opportunistic infections, slow healing, glucosuria

101
Q

What is an oral glucose tolerance test?

A
  • Baseline fasting plasma glucose taken
  • Give 75g glucose drink
  • Measure 2 hours later
  • Done before breakfast
102
Q

What is the diagnostic criteria for pre-diabetes?

A
  • HbA1C-> 42-47mmol/L
  • Impaired fasting glucose-> 6.1-6.9mmol/L
  • Impaired glucose tolerance test-> 7.8-11.1mmol/L at 2 hours
103
Q

What is the diagnostic criteria for diabetes?

A
  • HbA1C-> >48mmol/L
  • Random glucose-> >11mmol/L
  • Fasting glucose-> >7mmol/L
  • OGTT >11mmol/L at 2 hours
104
Q

What is the general management of type 2 diabetes?

A
  • Risk factor modifications
  • 1st line metformin 500mg then titrate up
  • 2nd line-> add SU or pioplitazone or DPP-4i or SGLT-2i
  • 3rd line-> triple therapy or metformin + insulin
105
Q

How does metformin work?

A

Biguanide-> increases insulin sensitivity + decrease liver production of glucose

106
Q

What are the side effects of metformin?

A
  • Lactic acidosis, GI (diarrhoea, abdominal pain)

- Not weight change or hypoglycaemia

107
Q

How does pioglitazone work?

A

Thiazolidinedione-> increase insulin sensitivity + decrease liver production of glucose

108
Q

What are the side effects of pioglitazone?

A
  • Weight gain, fluid retention, anaemia, heart failure, risk of bladder cancer
  • Not hypoglycaemia
109
Q

How do sulphonylureas work?

A

Stimulate insulin release

110
Q

What are the side effects of sulphonylureas?

A

Increased CVD and MI risk, weight gain, hypoglycaemia

111
Q

How do glucagon-like peptide-1 (GLP1) drugs work?

A
  • Incretin hormones produced by GI tract in response to large meals
  • Increases insulin secretion, inhibits glucagon production, slow absorption in the GI tract
112
Q

What are the side effects of glucagon-like peptide-1 (GLP1) drugs?

A

GI tract upset, weight loss, dizziness, low risk of hypos

113
Q

How do DPP-4 inhibitors work?

A
  • Inhibit dipeptidyl peptidase-4 enzyme-> increases GLP-1 activity
  • Increase insulin secretion + inhibit glucagon production
114
Q

What are the side effects of DPP-4 inhibitors?

A

GI tract upset, URTI symptoms, pancreatitis

115
Q

How do SGLT-2 inhibitors work?

A
  • SGLT-2 is a protein that helps glucose get reabsorbed from urine to blood in proximal tubules
  • Inhibit this-> glucose excreted in urine
116
Q

What are the side effects of SGLT-2 inhibitors?

A

Glucosuria, DKA, lower limb amputation, increased UTIs, weight loss

117
Q

What is an example of a sulphonylurea?

A

Gliclazide

118
Q

What is an example of a GLP-1 mimetic?

A

Exenatide

119
Q

What is an example of a DPP-4 inhibitor?

A

Sitagliptin

120
Q

What are some examples of SGLT-2 inhibitors?

A

Empagliflozin, dapagliflozin, canagliflozin

121
Q

What is an example of a rapid acting insulin?

A

Novorapid, Humalog

122
Q

How long does it take for rapid-acting insulin to act and how long does it last for?

A
  • Works in 10 minutes

- Lasts 4 hours

123
Q

How long does it take for short acting insulin to act and how long does it last for?

A
  • Works in 30 minutes

- Lasts 8 hours

124
Q

What are examples of short-acting insulins?

A

Actarapid, Humulin S

125
Q

What are examples of intermediate acting insulins?

A

Insulatard, Humulin I

126
Q

How long does it take for intermediate-acting insulin to act and how long does it last for?

A
  • Works in 1 hour

- Lasts 16 hours

127
Q

What are examples of long-acting insulins?

A

Levemir, degludec

128
Q

How long does it take for long-acting insulin to act and how long does it last for?

A
  • Works in 1 hour
  • Usually lasts 24 hours
  • Degludec-> lasts 40+ hours
129
Q

What are examples of combination insulins?

A
  • Rapid + intermediate acting
  • Humalog 25 (25:75)
  • Novomix (30:70)
130
Q

What is acromegaly?

A

Excess growth hormone produced by the anterior pituitary causes symptoms

131
Q

What causes acromegaly?

A
  • Excess growth hormone
  • Pituitary adenoma-> microscopic or significant
  • Ectopic GHRH or GH production from cancer
132
Q

Why do you get visual problems in acromegaly?

A

Optic chiasm above pituitary gland (where optic nerves cross over)-> pituitary tumour press on this-> bitemporal hemianopia (outer half of both eyes)

133
Q

What visual defect is common in acromegaly?

A

Bitemporal hemianopia-> lose vision in outer half of both eyes

134
Q

How does acromegaly present?

A
  • Space occupying lesion-> headaches + bitemporal hemianopia (outer half of both eyes)
  • Tissue overgrowth-> frontal bossing, large nose/hands/feet, macroglossia, prognathism (protruding jaw), arthritis
  • Organ dysfunction-> hypertrophy of heart, HTN, T2DM, colorectal cancer
  • New skin tags
  • Profuse sweating
135
Q

How is acromegaly investigated?

A
  • IGF-1 screen-> raised
  • OGGT + measure GH-> high glucose normally suppresses GH
  • MRI-> pituitary tumour
  • Ophthalmology-> formal visual field testing
136
Q

How is acromegaly managed?

A
  • Trans-sphenoidal pituitary adenoma removal
  • Remove cancer if ecpotic
  • Pegvisomant-> GH antagonist (SC daily)
  • Octreotide-> somatostatin analogue (inhibits GH release)
  • Bromocriptine-> dopamine agonist (inhibit GH)
137
Q

What are the key tests for diagnosing acromegaly?

A
  • IGF1 level

- Growth hormone suppression test (using OGTT)

138
Q

Which cells produce parathyroid hormone and in response to what?

A

Chief cells in the parathyroid glands-> in response to hypocalcaemia

139
Q

What is the function of parathyroid hormone?

A
  • Increase osteoclast activity in bones-> reabsorb calcium from bones
  • Increase calcium absorption in gut + kidneys
  • Increase vitamin D activity by converting to active form-> increase calcium absorption from intestines
140
Q

What are the signs and symptoms of hypercalcaemia?

A
  • STONES-> renal
  • BONES-> pain
  • GROANS-> abdominal pain, constipation, nausea, vomiting
  • MOANS-> psych ie fatigue, depression, psychosis
141
Q

What causes primary hyperparathyroidism?

A

Uncontrolled PTH due to gland tumours-> hypercalcaemia

142
Q

How do you treat primary hyperparathyroidism?

A

Surgical removal of parathyroid tumours

143
Q

What is the pathophysiology of secondary hyperparathyroidism?

A
  • Low vitamin D or CKD-> low calcium absorption
  • PT glands secrete more PTH in response to hypocalcaemia
  • Increased need of PTH-> total cells in PT glands increase-> hyperplasia
144
Q

What blood results will you get in secondary hyperparathyroidism?

A
  • Low/normal serum calcium

- High PTH

145
Q

How do you treat secondary hyperparathyroidism?

A
  • Correct vitamin D levels

- Renal transplant for CKD

146
Q

What causes tertiary hyperparathyroidism?

A
  • Long-standing secondary hyperparathyroidism-> hyperplasia

- Causes baseline PTH to be high even when treat underlying cause of secondary

147
Q

What does tertiary hyperparathyroidism cause?

A

Hypercalcaemia-> high absorption in intestine/kidneys/bones

148
Q

How is tertiary hyperparathyroidism managed?

A

Surgical removal of some PT tissue-> return bloods to normal level

149
Q

What blood results will you get in primary hyperparathyroidism?

A
  • High PTH

- High calcium

150
Q

What blood results will you get in tertiary hyperparathyroidism?

A
  • High PTH

- High calcium

151
Q

What is primary hyperaldosteronism?

A

AKA Conn’s syndrome-> adrenal glands produce too much aldosterone (usually due to adrenal adenoma)

152
Q

What causes primary hyperaldosteronism (AKA Conn’s syndrome)?

A
  • Adrenal adenoma
  • Bilateral adrenal hyperplasia
  • Familial hyperaldosteronism types 1 + 2
  • Adrenal carcinoma
153
Q

How does hyperaldosteronism present?

A

High BP not responding to treatment

154
Q

What is the pathophysiology of secondary hyperaldosteronism?

A

Excess renin stimulates adrenals to produce more aldosterone-> usually when BP of kidneys lower than rest of body (eg renal artery stenosis)

155
Q

What can cause secondary hyperaldosteronism?

A
  • High renin due to BP being lower in kidneys than rest of body
  • Renal artery stenosis
  • Renal artery obstruction
  • Heart failure
156
Q

What is renal artery stenosis?

A

Narrowing of the renal artery due to atherosclerotic changes

157
Q

How is renal artery stenosis diagnosed?

A
  • Doppler US
  • CT angiography
  • MRA-> MR angiography
158
Q

How is hyperaldosteronism investigated?

A
  • Serum renin:aldosterone ratio
  • BP-> high
  • Hypokalaemia
  • Blood gas-> alkalosis
  • Imaging for renal artery stenosis-> doppler US, CT/MR angiography
159
Q

How is hyperaldosteronism managed?

A
  • Treat underlying cause-> remove adenoma (primary) or percutaneous renal artery angioplasty (secondary due to stenosis)
  • Aldosterone antagonists-> spironolactone or eplerenone
160
Q

What blood results might you expect in primary hyperaldosteronism (Conn’s syndrome)?

A

High aldosterone + low renin

161
Q

What blood results might you expect in secondary hyperaldosteronism?

A

High aldosterone + high renin

162
Q

What is the pathophysiology behind syndrome of inappropriate anti-diuretic hormone (SIADH)?

A
  • ADH (vasopressin) produced in hypothalamus + secreted in posterior pituitary-> stimulate water reabsorption in collecting ducts
  • Too much-> excess water reabsorption + dilutes sodium-> hyponatraemia
  • Not enough to cause fluid overload-> euvolaemic hyponatraemia
  • Causes high urine osmolality + sodium-> more concentrated urine
163
Q

What are the symptoms of syndrome of inappropriate anti-diuretic hormone (SIADH)?

A
  • Non specific-> headache, fatigue, muscle aches, confusion

- Severe hyponatraemia-> seizures, LOC

164
Q

What can cause syndrome of inappropriate anti-diuretic hormone (SIADH)?

A
  • Post-op
  • Head injury
  • Infections-> atypical pneumonia
  • Meds-> thiazide diuretics, carbamazepine, antipsychotics, NSAIDs
  • Malignancy-> SCLC
  • Meningitis
165
Q

How is syndrome of inappropriate anti-diuretic hormone (SIADH) diagnosed?

A
  • Examination-> euvolaemic
  • Bloods-> hyponatraemia
  • Urine-> high osmolality + sodium
  • Exclude other causes-> short synacthen test, no diuretics, no diarrhoea/burns/sweating, no excess water, no AKI/CKD
  • Establish cause-> new meds, CXR, CT-TAP or MRI brain (malignancy)
166
Q

How is syndrome of inappropriate anti-diuretic hormone (SIADH) managed?

A
  • Treat underlying cause-> stop meds
  • Correct sodium slowly-> prevent central pontine myelinolysis
  • Fluid restriction-> 500ml-1L
  • Medical-> tolvaptan (ADH receptor blocker) or demeclocycline (inhibits ADH)
167
Q

Why is it important to correct sodium slowly in syndrome of inappropriate anti-diuretic hormone (SIADH)?

A

Prevent central pontine myelinolysis

168
Q

What is central pontine myelinolysis?

A
  • AKA osmotic demyelination syndrome
  • When long term hyponatraemia is corrected too quickly
  • Water rapidly shifts out of the brain
  • Can cause neurological deficits long term
169
Q

What is the pathophysiology of central pontine myelinolysis?

A
  • Water moves by osmosis across BBB from low conc to high conc-> from blood to brain when low serum level
  • Long term hyponatraemia (<120mmol/L)-> brain adapts to oedema by reducing soluted in cells-> water balances across BBB over a few days
  • Treated at >10mmol/L increase over 24 hours-> too quick
  • Water rapidly shifts from brain (low conc) to blood (high conc)
  • Causes demyelination especially in pons-> few days after correction)
170
Q

What are the symptoms of central pontine myelinolysis?

A
  • 1st phase-> confused + N+V due to electrolyte imbalance
  • 2nd phase (demyelination)-> spastic quadraparesis, pseudobulbar palsy, cognitive + behaviour change, risk of death
  • Often left with neuro deficit
171
Q

How is central pontine myelinolysis managed?

A

Supportive-> often can’t cure

172
Q

What is diabetes insipidus?

A
  • Lack of response to ADH-> prevents kidneys concentrating urine-> polyuria + polydipsia
  • Nephrogenic-> collecting ducts not responding
  • Cranial-> hypothalamus not producing ADH so pituitary gland not secreting
173
Q

What causes nephrogenic diabetes insipidus?

A
  • Collecting ducts not responding to ADH
  • Side effect of lithium
  • Hypokalaemia or hypercalcaemia
  • Genetic diseases eg AVRP2 gene
174
Q

What causes cranial diabetes insipidus?

A
  • Hypothalamus not produce ADH for pituitary gland to secrete
  • Idiopathic
  • Brain tumour
  • Head injury
  • Malformations
  • Infection-> meningitis, encephalitis, TB
  • Surgery
  • Radiotherapy
175
Q

How does diabetes insipidus present?

A

Polyuria, polydipsia, hypernatraemia, dehydration, postural hypotension

176
Q

How is diabetes insipidus investigated?

A
  • Water deprivation test (AKA desmopressin stimulation test)
  • Urine-> low osmolality
  • Blood-> high osmolality
177
Q

What is the investigation of choice for diabetes insipidus?

A

Water deprivation test (AKA desmopressin stimulation test)

178
Q

How does the water deprivation test (AKA desmopressin stimulation test) work?

A
  • Avoid fluid for 8 hours + measure urine osmolality
  • Give desmopressin (synthetic ADH) + measure urine osmolality 8 hours later
  • Cranial DI-> low osmolality after deprivation + high after ADH
  • Nephrogenic DI-> low osmolality after deprivation + low after given ADH
179
Q

What result would you expect in cranial diabetes insipidus after a water deprivation test and why?

A
  • Low osmolality after deprivation + high after ADH

- Lacks ADH and kidneys work so reabsorb water + concentrate urine after given ADH

180
Q

What result would you expect in nephrogenic diabetes insipidus after a water deprivation test and why?

A
  • Low osmolality after deprivation + low after given ADH

- Kidneys unable to respond to ADH

181
Q

How is diabetes insipidus managed?

A
  • May not need any if mild
  • Treat underlying cause
  • Desmopressin (synthetic ADH)-> in cranial usually
182
Q

What is a phaeochromocytoma?

A

A tumour of the adrenal medulla that causes unregulated + excess adrenaline secretion

183
Q

Where is adrenaline produced?

A

Chromaffin cells in the adrenal medulla

184
Q

What is the pathophysiology of phaeochromocytoma?

A
  • Tumour of adrenal medulla-> can be in multiple endocrine neoplasia type 2
  • Excess adrenaline released in bursts-> stimulates sympathetic nervous system
  • 10% rules-> 10% bilateral, 10% cancer, 10% outside of adrenals
185
Q

How is phaeochromocytoma diagnosed?

A
  • 24 hour urine catecholamines-> secreted by tumour

- Plasma free metanephrines-> longer half life than adrenaline

186
Q

How does phaeochromocytoma present?

A
  • Peaks + troughs of symptoms

- Anxiety, sweating, headache, HTN, palpitations, tachycardia, paroxysmal AF

187
Q

How is phaeochromocytoma managed?

A
  • Adrenalectomy to remove tumour-> when symptoms controlled to reduce risks of surgery + GA
  • Phenoxybenzamine-> alpha blocker
  • Beta blockers-> later down line
188
Q

What is hyperosmolar hyperglycaemic state?

A

Profound hyperglycaemia without ketouria or ketoacidosis-> usuallt in T2DM

189
Q

How is hyperosmolar hyperglycaemic state diagnosed?

A
  • Symptoms-> similar to DKA
  • Blood glucose-> often >30mmol/L
  • Bloods-> hyperosmolar + thick (>320mgHM/kg)
190
Q

How is hyperosmolar hyperglycaemic state managed?

A
  • IV saline-> aim for +ve fluid balance of over 3L by 12 hours
  • IV insulin-> 0.05units/kg, when glucose no longer falling with IV saline
  • Bring down sodium <10mmol/L in 24 hours-> reduce cerebral oedema risk
  • Monitor for cerebral oedema-> neuro exams, GCS etc

Medicine (13 decks)

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